【摘要】 目的应用血管紧张素II刺激致新生SD大鼠心肌细胞肥厚,探讨参三七皂甙Rg1(Rg1)对缺氧复氧(H/R)损伤的保护作用及机制。方法用AngII刺激致乳鼠(SD大鼠)心肌细胞肥厚,细胞H/R损伤前48h给予Rg10.01～10.00μmol/L预适应处理,检测各组心肌细胞表面积和细胞蛋白含量,测定心肌细胞凋亡率、细胞生存能力和培养液中乳酸脱氢酶、丙二醛及一氧化氮含量。结果与H/R损伤组相比,Rg10.01～10.00μmol/L预适应组细胞表面积和蛋白含量分别减少47.92%和46.99%;细胞生存率增加37.98%,细胞凋亡率降低85.29%;乳酸脱氢酶活性和丙二醛含量分别降低56.25%和70.78%,一氧化氮含量增加2.6倍。结论Rg1预适应可显著减轻AngII致肥厚心肌细胞缺氧复氧损伤,增强受损细胞生存能力,机制与抑制细胞凋亡、减少乳酸脱氢酶释放、增强一氧化氮活性,减少脂质过氧化有关。更多还原

【Abstract】 Aim To study the effects of preconditioning of Panax notoginsenoside Rg1(Rg1)on neonatal rat cardiomyocytes against hypoxia reoxygenation(H/R) injury and its mechanisms.Methods Myocyte hypertrophy model was induced by Angiotensin II in neonatal and determined by the cell surface area and total protein content of cardiomyocytes.The H/R model was established after treatment with Rg1 for 48 h.The cell survival ability was assayed by MTT method.The cell surface area of cardiomyocytes was measured by confocal microscopy.The apoptotic rate was assayed by flow cytometry. Total protein content in myocytes ,the activities of lactate dehydrogenase (LDH), content of nitric oxide(NO)and malondialdehyde (MDA) in medium were measured.Results After treatment of cells with Rg1(0.01～10.00μmol / L) for 48 h, compared with H/R group, the myocyte cell surface area was reduced by 47.92 %, the total protein content was lowered by 46.99%;the LDH activity was reduced by 56.25 %, the content of MDA were lowered by 70.78 %,the cell survival was increased by 37.98%and the apoptosis rate reduced by 85.29 %; NO content enhanced by 2.6 fold.Conclusion Panax notoginsenosideRg1 pretreatment protects hypertrophy myocardium mduced by AngII against hypoxia reoxygenation injury,increase myocyte viability and lower total protein content,and this effect is related to reducing apoptosis,reducing the release of LDH, improving content of nitric oxide and lowering the level of lipid peroxidation.更多还原